Three-dimensional changes in left and right ventricular geometry in
chronic mitral regurgitation.
Young, Alistair A., Roger Orr, Bruce H. Smaill, Louis J. Dell'italia.
Department of Physiology, [tilde]n Department of Anatomy with
Radiology, School of Medicine, University of Auckland, Private Bag
92019, Auckland, New Zealand, [acute]a Birmingham Veteran Affairs
Medical Center, University of Alabama at Birmingham, Department of
Medicine, Division of Cardiology, University Station, Birmingham,
Alabama 35294 and Auburn University College of Veterinary Medicine,
Auburn, Alabama 36849-5525
APStracts 3:0278H, 1996.
Regional three dimensional (3D) right and left ventricular geometry
was studied in eight dogs before, and five to six months after,
induction of mitral regurgitation (MR). Ventricular shape changes
were quantified using a 3D finite element model fitted to chamber
contours traced on cardiac magnetic resonance images. MR increased LV
EDV (99 vs 57 ml, p&LT0.001) and LV stroke volume (SV) (55 vs 26
ml, p &LT 0.001). In contrast, right ventricular EDV decreased (45
vs 55 ml, p &LT 0.01) while SV was maintained. LV mass (free wall
plus septum) increased (115 vs 94 g, p&LT0.05), whereas RV free
wall mass was relatively unchanged. Shape changes due to MR were
characterized by a marked (7.4 mm) rightward shift of the septum
relative to the lateral LV free wall at end-diastole. In contrast,
the distance from RV free wall to lateral LV free wall was relatively
unchanged (2.7 mm). The distance between the LV lateral free wall and
septum increased more than the distance between the anterior and
posterior LV walls (22% vs 15%, p=0.04). During systole, the
displacement of the septum into the LV increased significantly (7.3
vs 2.9 mm, p &LT 0.01). Consistent with the end-diastolic
dimension changes, LV endocardial circumferential curvature was
decreased at end-diastole to a greater extent in anterior and
posterior walls than in septal and lateral walls (p&LT0.01). Thus,
chronic MR produced an asymmetric LV dilatation with regional
variation in geometry. The septum increased its contribution to the
LV SV at the expense of RV EDV. RV SV was maintained, possibly by
ventricular interaction.
Received 30 October 1995; accepted in final form 5 June 1996.
APS Manuscript Number H1015-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996